The left atrial appendage (LAA) originates from the left wall of the left atrium. This fingerlike projection opens to the atrium through an ovoid orifice and extends 2-4 cm long, pointing towards the apex.
Atrial fibrillation (AF) is the most common arrhythmia (i.e. irregularly timed contraction) and oftentimes occurs due to sustained increased left atrial afterload—leading to an enlargement of the left atrium (LA). The presence of AF may establish a positive feedback loop that furthers enlargement and increases the probability of thrombus (i.e. clotting) formation. As the LAA is not contracting on time, blood stasis occurs in the appendage as the blood flows into the appendage but does not flow out in a rhythmic fashion. This leads to blood clotting in the appendage, which then becomes a risk as the irregular contraction of the LAA may force the clot to travel out of the appendage and into the brain, leading to an ischemic stroke.
It is believed by researchers that up to 90 percent of the clots found in the brain come from the LAA. If AF patients are not treated, their risk of stroke increases as they age; 15 percent of all strokes are caused by AF. However, in patients 70 years and older, more than 20 to 25 percent of strokes are caused by atrial fibrillation.
Current research suggests that occlusion of the left atrial appendage reduces the risk of ischemic stroke in atrial fibrillation patients by preventing LAA thrombus formation from occurring. It also acts as an alternative therapy to oral anticoagulation (OAC). Some patients elect to not take OACs or are ineligible due to side effects.